PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34121490-8 2021 However, compared to that in the DEX + H2O2 group, cell viability in the mimic + DEX + H2O2 group was decreased, and the apoptotic rate was elevated with increased cleaved caspase-3 and decreased Bcl-2 expression. Dexmedetomidine 33-36 BCL2, apoptosis regulator Rattus norvegicus 196-201 34121490-7 2021 In addition, both DEX and miR-134 inhibitor reduced the upregulated expression of cleaved caspase-3 and increased the downregulated expression of Bcl-2 in H2O2-induced PC12 cells. Dexmedetomidine 18-21 BCL2, apoptosis regulator Rattus norvegicus 146-151 34121490-8 2021 However, compared to that in the DEX + H2O2 group, cell viability in the mimic + DEX + H2O2 group was decreased, and the apoptotic rate was elevated with increased cleaved caspase-3 and decreased Bcl-2 expression. Dexmedetomidine 81-84 BCL2, apoptosis regulator Rattus norvegicus 196-201 34135573-10 2021 However, DEX (>=100 muM) downregulated the protein expression of Bcl-2, decreased the mitochondrial membrane potential (MTP), and reduced ATP synthesis. Dexmedetomidine 9-12 BCL2, apoptosis regulator Rattus norvegicus 65-70 35459107-10 2022 RESULTS: Post-MV, compared with group OLV, group DEX showed increases in percentage of target quadrant time (P < 0.05), platform crossings (P < 0.05), a reduction in CERO2 (P < 0.05), and pERK1/2, pCREB, and Bcl-2 significantly increased (P < 0.01 or P < 0.05), while BAX significantly decreased (P < 0.01), besides, a less damaged synaptic structure was observed in group DEX. Dexmedetomidine 49-52 BCL2, apoptosis regulator Rattus norvegicus 208-213 35527005-10 2022 DEX attenuated the increase in the levels of NE, ALT, AST, MDA, ROS, apoptosis, SOD2, COX-2, Cytochrome C, cleaved caspase 3, Bax, and P-JNK, P-p38, c-AMP, P-PKA and miR-34a-5p, and the decrease in the levels of SOD, GPX, GSH and Bcl-2 in model rats. Dexmedetomidine 0-3 BCL2, apoptosis regulator Rattus norvegicus 230-235 33220608-11 2021 Dexmedetomidine significantly decreased protein expressions of IRAK1, TRAF6, cleaved Caspase-3, BAX, and NF-kappaB p65, but increased expressions of BCL-2 in H9C2 cells. Dexmedetomidine 0-15 BCL2, apoptosis regulator Rattus norvegicus 149-154 33220608-12 2021 miR-146a-3p overexpression strengthened the anti-apoptotic effect induced by dexmedetomidine in H9C2 cells via decreasing protein levels of IRAK1, TRAF6, cleaved Caspase-3, BAX, NF-kappaB p65, p-NF-kappaB p65, and p-IkappaBalpha and increasing protein level of BCL-2. Dexmedetomidine 77-92 BCL2, apoptosis regulator Rattus norvegicus 261-266 33280824-9 2021 CONCLUSION: Dexmedetomidine suppresses hepatic IR injury and the protective mechanism appears to involve the decrease of IL-6 and upregulation of Bcl-2 expression, which result in the attenuation of inflammatory response and the inhibition of apoptosis. Dexmedetomidine 12-27 BCL2, apoptosis regulator Rattus norvegicus 146-151 33173983-7 2020 Dex significantly attenuated the ratio of Bak/Bcl-2, cleaved caspase-3 expression levels and epithelial cell death, and increased the expression of phosphorylated ERK1/2. Dexmedetomidine 0-3 BCL2, apoptosis regulator Rattus norvegicus 46-51 32419697-13 2020 Moreover, DEX notably reduced expressions of caspase-3, caspase-9, cyt-c, and bax and increased expression of bcl-2. Dexmedetomidine 10-13 BCL2, apoptosis regulator Rattus norvegicus 110-115 32407987-6 2020 Furthermore, immunohistochemical staining and western blot analysis revealed that DEX pretreatment significantly increased the I/R-induced expression levels of B-cell lymphoma 2 (Bcl-2), phosphorylated phosphoinositide 3-kinase (pPI3K) and pAkt, and significantly decreased those of pBcl-2 associated agonist of cell death, Bcl-2-associated X protein and cleaved caspase 3 in vivo and in vitro. Dexmedetomidine 82-85 BCL2, apoptosis regulator Rattus norvegicus 160-177 32407987-6 2020 Furthermore, immunohistochemical staining and western blot analysis revealed that DEX pretreatment significantly increased the I/R-induced expression levels of B-cell lymphoma 2 (Bcl-2), phosphorylated phosphoinositide 3-kinase (pPI3K) and pAkt, and significantly decreased those of pBcl-2 associated agonist of cell death, Bcl-2-associated X protein and cleaved caspase 3 in vivo and in vitro. Dexmedetomidine 82-85 BCL2, apoptosis regulator Rattus norvegicus 179-184 32655771-5 2020 Dexmedetomidine treatment upregulated the expression of CB2 receptor and suppressed the I/R-induced increases in lung injury scores, inflammatory cell infiltration, lung wet/dry ratio, MPO activity, MDA level, inflammatory cytokines, and caspase-3 expression while augmenting SOD activity and Bcl-2 expression, indicating attenuation of lung injury. Dexmedetomidine 0-15 BCL2, apoptosis regulator Rattus norvegicus 293-298 29749492-11 2018 The expression of Bcl-2 was increased in the dexmedetomidine treated rats, compared with that in the control group. Dexmedetomidine 45-60 BCL2, apoptosis regulator Rattus norvegicus 18-23 32034118-8 2020 Dexmedetomidine significantly reduced the expression of caspase-3 in the rat lung tissue (P<0.01), and significantly increased the expression of Bcl-2/Bax and the phosphorylation levels of AMPK, SIRT1, nuclear factor-kappaB (NF-kappaB), and forkhead box class O 3a (FOXO3a). Dexmedetomidine 0-15 BCL2, apoptosis regulator Rattus norvegicus 145-150 31680420-4 2020 Dexmedetomidine administration at the beginning of reperfusion or reoxygenation attenuated I/R-induced myocardial injury or H/R-induced cell death, alleviated mitochondrial dysfunction, reduced the number of apoptotic cardiomyocytes, inhibited the activation of HIF-1alpha and modulated the expressions of apoptosis-related proteins including BCL-2, BAX, BNIP3, cleaved caspase-3 and cleaved PARP. Dexmedetomidine 0-15 BCL2, apoptosis regulator Rattus norvegicus 343-348 31308624-10 2019 In addition, DEX dose-dependently reduced apoptotic PC12 cells induced by lidocaine,as reflected by the decreased expression of apoptosis-related Bax, caspase-3 and caspase-9 and increased expression of anti-apoptotic Bcl-2 compared to the cells only treated with lidocaine. Dexmedetomidine 13-16 BCL2, apoptosis regulator Rattus norvegicus 218-223 30402501-10 2018 The phosphorylation of Akt and GSK-3beta was increased, Bcl-2 mRNA and the Bcl-2/Bax ratio was increased, and Bax mRNA was decreased in the DEX group as compared to the I/R group, while posttreatment with Wort attenuated the effects induced by DEX. Dexmedetomidine 140-143 BCL2, apoptosis regulator Rattus norvegicus 56-61 30402501-10 2018 The phosphorylation of Akt and GSK-3beta was increased, Bcl-2 mRNA and the Bcl-2/Bax ratio was increased, and Bax mRNA was decreased in the DEX group as compared to the I/R group, while posttreatment with Wort attenuated the effects induced by DEX. Dexmedetomidine 140-143 BCL2, apoptosis regulator Rattus norvegicus 75-80 31635678-8 2020 Dex inhibited I/R injury by decreasing apoptosis significantly with rescue of cleaved caspase-3 and the Bcl-2/Bax ratio. Dexmedetomidine 0-3 BCL2, apoptosis regulator Rattus norvegicus 104-109 31220473-8 2019 Dexmedetomidine ameliorated KA-induced apoptosis, and this neuroprotective effect was accompanied by inhibited the KA-induced caspase-3 expression as well as MAPKs phosphorylation, and reversed Bcl-2 down-expression, coupled with increased Nrf2, BDNF and TrkB expression in KA-treated rats. Dexmedetomidine 0-15 BCL2, apoptosis regulator Rattus norvegicus 194-199 31220473-9 2019 The results suggest that dexmedetomidine protected rat brains from KA-induced excitotoxic damage by reducing glutamate levels, suppressing caspase-3 activation and MAPKs phosphorylation, and enhancing Bcl-2, Nrf2, BDNF and TrkB expression in the hippocampus. Dexmedetomidine 25-40 BCL2, apoptosis regulator Rattus norvegicus 201-206 31511215-10 2019 In the diabetic rats with renal IR injury, Dex treatment prior to the injury significantly lowered the expressions of Scr, BUN, p-eNOS, eNOS, cleaved caspase-3, and Bax, decreased the percentage of apoptotic cells, and increased the levels of HIF-1a and Bcl-2 (P &lt; 0.05). Dexmedetomidine 43-46 BCL2, apoptosis regulator Rattus norvegicus 254-259 31511215-11 2019 Digoxin treatment significantly antagonized the effects of Dex in the diabetic rats with renal IR injury by increasing the expressions of cleaved caspase-3 and Bax, promoting glomerular cell apoptosis, and decreasing renal expressions of HIF-1 and Bcl-2 (P &lt; 0.05). Dexmedetomidine 59-62 BCL2, apoptosis regulator Rattus norvegicus 248-253 30655009-10 2019 Dexmedetomidine preconditioning also increased the Bcl-2 level (0.55+-0.04 vs. 0.34+-0.05, p<0.05) and decreased the level of Bax (0.46+-0.03 vs. 0.68+-0.04, p<0.05), caspase-3 (0.49+-0.03 vs. 0.69+-0.04, p<0.05). Dexmedetomidine 0-15 BCL2, apoptosis regulator Rattus norvegicus 51-56 27959438-6 2017 In addition, DEX treatment markedly prevented the LPS-induced mitochondrial-dependent apoptotic pathway in vitro (increases of cell apoptotic rate, cytosolic cytochrome c, and caspase 3 activity) and in vivo (increases of terminal deoxynucleotidyl transferase dUTP nick-end labeling positive cells, cleaved caspase 3, Bax upregulation and Bcl-2 downregulation). Dexmedetomidine 13-16 BCL2, apoptosis regulator Rattus norvegicus 340-345 29693126-7 2018 The results of the present study revealed that administration of Dex post-TBI improved brain edema and neurological outcomes, due to the attenuation of the TBI-induced reduction of Bax expression and increase of Bcl-2 and HSP70 expression. Dexmedetomidine 65-68 BCL2, apoptosis regulator Rattus norvegicus 212-217 28436683-7 2017 Taken together, dexmedetomidine may protect PC12 cells from lidocaine-induced cytotoxicity through miR-let-7b and COL3A1, while also increasing Bcl2 and inhibiting caspase 3. Dexmedetomidine 16-31 BCL2, apoptosis regulator Rattus norvegicus 144-148 28463790-8 2017 Mechanistically, DEX activated the mitogen-activated protein kinase (MAPK) pathway, impaired caspase-3 expression, and enhanced anti-apoptotic factor Bcl-2 to resist lidocaine-induced apoptosis, indicating that the optimal dose of DEX alleviates lidocaine-induced cytotoxicity and should be considered in clinical application. Dexmedetomidine 17-20 BCL2, apoptosis regulator Rattus norvegicus 150-155 27571870-9 2016 Dexmedetomidine treatment (0.001-100 microM) of the neurons prior to propofol exposure attenuated the propofol-induced neuronal apoptosis and increased expression levels of BDNF, Bcl-2 and p-CREB compared with the propofol only group. Dexmedetomidine 0-15 BCL2, apoptosis regulator Rattus norvegicus 179-184 27571870-11 2016 These in vitro data indicated that dexmedetomidine exerted direct neuroprotective effects to prevent cultured hippocampal neuronal injury caused by propofol, accompanied by an increase in the levels of p-CREB, Bcl-2 and BDNF. Dexmedetomidine 35-50 BCL2, apoptosis regulator Rattus norvegicus 210-215 12538207-8 2003 In animals treated with dexmedetomidine, the expression of Bcl-2 and Mdm-2 was larger compared with control (68% and 210%, respectively) or sham-operated (110% and 180%, respectively) animals. Dexmedetomidine 24-39 BCL2, apoptosis regulator Rattus norvegicus 59-64 25026397-9 2014 Dexmedetomidine pretreatment inhibited isoflurane-induced neuroapoptosis and restored proteins expression of MAPK pathways and the Bcl-2/Bax ratio after isoflurane exposure. Dexmedetomidine 0-15 BCL2, apoptosis regulator Rattus norvegicus 131-136 20003127-10 2010 Isoflurane treatment decreased Bcl-2 and pERK protein expression relative to air, an effect reversed by dexmedetomidine treatment. Dexmedetomidine 104-119 BCL2, apoptosis regulator Rattus norvegicus 31-36 27221008-13 2016 Compared with the I/R group, the ratio of Bcl-2/Bax at the mRNA level was elevated in the DEX and ischemic post-conditioning groups, whereas the expression levels of Bax were decreased. Dexmedetomidine 90-93 BCL2, apoptosis regulator Rattus norvegicus 42-47 27069541-9 2016 Compared with the model group, rats given Dex had (1) shorter escape latencies, (2) more platform crossings, (3) fewer relaxin-3 and c-fos positive neurons in the hippocampal CA1 area, (4) upregulation of Bcl-2, (5) downregulation of Fas, caspase-8, and caspase-9 proteins, and (6) decreased neuroapoptosis in the hippocampus. Dexmedetomidine 42-45 BCL2, apoptosis regulator Rattus norvegicus 205-210 26622369-12 2015 In addition, DEX treatment resulted in a reduction in the expression levels of Bax in the intestinal tissues, while increasing those of Bcl-2, in addition to significantly increasing the mRNA levels of telomerase and caspase-3. Dexmedetomidine 13-16 BCL2, apoptosis regulator Rattus norvegicus 136-141